Kawaguchi T, Asahi T, Satoh T, Uozumi T, Beppu T
J Antibiot (Tokyo). 1984 Dec;37(12):1587-95. doi: 10.7164/antibiotics.37.1587.
"Curing" treatment of a rifamycin-producing Nocardia sp. resulted in a mutant deficient in the synthesis of antibiotics. This deficiency was reversed in a medium containing yeast extract. The active substance, named B-factor, which induced rifamycin production in the mutant was purified from yeast extract, and its structure, 3'-(1-butylphosphoryl) adenosine, was determined by structural analysis and chemical synthesis. An extremely low concentration of B-factor (10 ng/ml) caused recovery of rifamycin B synthesis in the mutant and stimulated synthesis of the antibiotic in the parental strain.
对一株产利福霉素的诺卡氏菌进行“治愈”处理后,得到了一株抗生素合成缺陷的突变体。在含有酵母提取物的培养基中,这种缺陷得以逆转。从酵母提取物中纯化出了一种名为B因子的活性物质,它能诱导突变体产生利福霉素,通过结构分析和化学合成确定了其结构为3'-(1-丁基磷酰基)腺苷。极低浓度的B因子(10纳克/毫升)就能使突变体恢复利福霉素B的合成,并刺激亲本菌株合成抗生素。